Corilagin inhibits the proliferation of vascular smooth muscle and excessive matrix deposition following vascular injury via the MAPK pathway.

Corilagin is a type of ellagitannin that exhibits inhibitory effects on the proliferation of vascular smooth muscle cells (VSMCs). However, the mechanism underlying this inhibition remains unclear. The study utilized a balloon injury-induced rat carotid artery model to investigate the effects of corilagin on the prevention of restenosis following vascular injury. VSMCs were isolated from the carotid arteries of rats post-balloon injury and treated with PDGF-BB and various concentrations of corilagin. Western blotting was employed to assess the phosphorylation levels of MAPK in VSMCs. Two weeks of treatment with corilagin or a control vehicle was conducted on the injury model, and the area of neointima formation and collagen density in the intima were evaluated histopathologically. Our results revealed that corilagin dose-dependently inhibited VSMCs migration and phenotypic transformation, suppressing extracellular matrix deposition by upregulating matrix metalloproteinases (MMPs) and reducing collagen (COL) protein synthesis. In vivo, this result showed a significantly lower intimal thickness and intima/media ratio in the corilagin group compared to the control group. Corilagin inhibits the proliferation and migration of VSMCs by reducing the phosphorylation of ERK, p38, and JNK, and this effect can be weakened by the ERK/MAPK pathway activator C6 ceramide. Corilagin may be a promising drug that could provide a new approach to preventing and treating post-interventional restenosis.